Trace Element Deficiency in Cattle

Copper, cobalt and selenium/vitamin E, are considered the
important trace elements of cattle impacting on performance but
their role is often exaggerated by malnutrition, poor husbandry,
and ineffective parasite control.

Copper deficiency

Although it can occur as a primary deficiency on copper
deficient pastures, secondary copper deficiency is more common due
to antagonism by sulphur, iron and especially molybdenum in the
rumen. Two or more of these elements will act synergistically to
reduce available copper in the diet. Hence what may be considered a
'normal' concentration of these, acting together, can produce signs
of copper deficiency.

Fig 1: Trace element deficiency or winter coat?

Clinical presentation

Clinical signs of copper deficiency are usually seen in young
animals at pasture and manifest as poor growth rates.
De-pigmentation classically occurs as grey/brown discolouration of
the coat especially around the ear margins and eyes giving a
"spectacle-eye" appearance. Defective keratinisation can lead to
the formation of a thin, dry, sparse hair coat not to be confused
with the normal shedding of the winter coat. Widening of the growth
plates of the long bones of the legs is also seen-leading to signs
of lameness Diarrhoea is classically seen after turnout onto
pastures with high molybdenum concentrations - so called "teart
pastures". Anaemia occurs after prolonged and/or severe periods of
copper deficiency.

Copper deficiency has been associated with reduced fertility.
The most commonly linked presentation is depressed or delayed
oestrus behaviour, particularly in heifers. The evidence for other
effects in apparently normal animals, such as reduced conception
rates is even more equivocal. Impaired fertility is associated with
secondary copper deficiency due to high molybdenum intakes rather
than primary copper deficiency.

Fig 2: The diagnosis of copper deficiency is not
simple.

Fig 3: Cattle grazing "teart pastures" on the
Somerset levels.

Differential diagnoses of poor
growth

Malnutrition

Parasitic
gastroenteritis

Diarrhoea cause by
parasitic gastroenteritis (Type I ostertagiosis)

Diagnosis

Plasma copper concentrations - are suitable for the diagnosis of
clinical disease, but not for the estimation of body copper
reserves. A group of seven to 10 cattle should be sampled. Response
to supplementation as directed by the farmer's veterinary
practitioner is the most important indicator of deficiency. Liver
biopsy samples are the best samples to take to measure copper
reserves (and thus, for example, predict whether cattle are likely
to need supplementation to prevent deficiency in the future).
Samples from at least 6 animals are needed in most cases.

Treatment and prevention of
deficiency

Copper can be supplemented either
parenterally or orally. Injectable products have been used widely
in the past, principally because of their ease of use, but no
products licensed for use in cattle are currently available in the
UK. Use of the sheep product or of products imported from elsewhere
is not recommended.

Oral copper supplementation via the feed (either as a purchased
feed supplemented by the manufacturer or as a mineral added to the
feed on-farm) can be a very effective method of controlling copper
deficiency. An alternative to in-feed supplementation is the
use of slow release boluses. A range of products are available.
Some contain copper oxide needles which bypass the rumen and
dissolve in the acid environment of the true stomach (abomasum) to
give slow-release of copper over several months. Multi-mineral
boluses are also available; these contain copper alongside other
minerals. In these boluses copper is released into the
rumen/reticulum, over a period of 6-8 months (depending on the
product).

The best product for you depends on your farm system (especially
the type of stock you want to treat) and the reasons and causes of
mineral deficiency. Always get veterinary advice as to which regime
is best for your farm before starting a copper supplementation
programme.

Fig 4: Type I ostertagiosis in a Simmental cross
stirk.

Fig 5: Response to supplementation as directed by
the farmer's veterinary practitioner is the most important
indicator of deficiency.

Selenium and Vitamin E deficiency

Nutritional muscular dystrophy, White muscle
disease

Aetiology

Both selenium and Vitamin E play
key complimentary but independent roles to protect cells against
damage. Skeletal, cardiac and respiratory muscles are the most
susceptible to damage. Disease is more common in the progeny of
(beef) cows fed home-grown feeds from selenium deficient pastures
without appropriate mineral supplementation.

Fig 6: White muscle disease is more common in the
progeny of beef cows fed home-grown feeds from selenium deficient
pastures without appropriate mineral
supplementation.

Clinical presentation

The congenital form of selenium/vitamin E deficiency is seen
either as stillbirth, or the birth of a weak calf that is unable to
suck unaided and usually dies within a few days of
starvation/secondary bacterial infection.

The delayed form of selenium/vitamin E deficiency is usually
seen in calves between one and four months-old. Signs are usually
precipitated by sudden unaccustomed exercise typically following
turnout to pasture in the spring. The clinical appearance varies
according to the muscles affected.

Skeletal muscles
- there is sudden onset stiffness and inability to stand.
Otherwise, the calf is bright and alert with a normal appetite.

Respiratory muscles - the calf presents with
respiratory distress.

Cardiac muscle - there is sudden death without previous
signs of illness.

Fig 7: Selenium/vitamin E deficiency in a month-old
calf three days after turnout to pasture.

Sodium selenate or selenite may be given by injection, usually
combined with Vitamin E and will provide adequate selenium
supplementation for up to 3 months. The response to treatment may
take 4-7 days.

Prevention/control measures

Subcutaneous injections of barium selenate provide adequate
supplementation for 9-12 months. Oral dosing using 0.1 mg/kg sodium
selenate will provide adequate supplementation for 1-3 months.
Intra-ruminal soluble glass boluses provide slow release of
selenium for 6-12 months. Selenium and vitamin E are frequently
added to concentrate rations for feeding to cattle. The ingestion
of minerals varies greatly and this method is generally considered
to be an unreliable means of supplementing cattle.

Fig 8: Selenium and vitamin E are concentrated in
the colostrum therefore supplementation of the dam's diet during
late pregnancy will ensure good supply to the newborn
calf

Fig 9: The ingestion of minerals varies greatly and
this method is generally considered to be an unreliable means of
supplementing cattle.

Selenium can cross the placenta, and both selenium and
vitamin E are concentrated in the colostrum therefore
supplementation of the dam's diet during late pregnancy will ensure
good supply to the newborn calf.

Cobalt deficiency
(cobalt pine)

Aetiology

Cobalt deficiency is restricted to certain geographical areas
and is the direct result of ingestion of grass/crops grown on
cobalt deficient soils. All cattle require dietary cobalt for the
manufacture of vitamin B12. Note that cobalt deficiency
is very much less common in cattle than sheep.

Fig 10: Free access minerals!

Iodine
deficiency

Iodine is essential as a constituent of the thyroid hormones, in
particular T3 and T4, and 80 per cent of the
iodine in the body is found in the thyroid gland. Iodine deficiency
occurs sporadically in the UK.

Cause

Low iodine content in the soil leads to primary deficiency.
Secondary deficiency results from ingestion of the goitrogen
thiocyanate found in brassicas and legumes, and thiouracil found in
brassica seeds (e.g. some older varieties of oil-seed rape).
Selenium is required for the conversion of T4 to active
T3, and thus selenium deficiency may lead to secondary
iodine deficiency states.

Clinical presentation

The classical sign of iodine deficiency is thyroid enlargement
(goitre) due to compensatory mechanisms invoked by the lack of
thyroid hormone production. Calves born to iodine-deficient dams
may be stillborn, with goitre and areas of alopecia and
subcutaneous oedema. Weak calves are unwilling to suck causing high
perinatal mortality.

As with selenium, iodine deficiency has also been implicated in
poor growth rates, poor milk production and retained placenta.

Diagnosis

Severe goitre in calves will be detectable on clinical
examination. Thyroid weight (<10 g, normal; >13 g, abnormal),
fresh thyroid weight:body weight ratio (<0.5, normal; >1.0,
abnormal), and histopathology can be used to confirm the diagnosis.
Plasma inorganic iodine (PII) measures current daily iodine intake
(short-term), and is thus susceptible to changes in feed intake.
T4 levels reflect the thyroid and iodine status of the
animal (>50 nmol/l, normal; <20 nmol/l, abnormal), and are
useful in the diagnosis of deficiency. Care must be taken in
interpretation of T4 values, as there is natural
variation according to stage of lactation (levels are much lower in
early lactation), season, age of animal etc.

Treatment

Oral dosing using potassium iodide is relatively short-acting
and laborious. Intra-ruminal boluses provide slow release of iodine
for 6 months. Painting 5 per cent tincture of iodine onto the flank
skin-fold once a week in milking dairy cattle can work well, but is
too labour intensive in dry cows and beef animals. Free-access
minerals, medication of water supplies and pasture fertilisers can
all be used to varying effect.

Prevention/control measures

Iodine is frequently added to concentrate rations for feeding to
cattle, for example using seaweed preparations. Rapeseed meals are
usually treated to eliminate goitrogens prior to feeding, and newer
"double-zero" oil seed rape varieties are lower in goitrogens.

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